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Peripheral chemoreceptor
Peripheral chemoreceptors (of the carotid and aortic bodies) are so named because they are sensory extensions of the peripheral nervous system into blood vessels where they detect changes in chemical concentrations. As transducers of patterns of variability in the surrounding environment, carotid and aortic bodies count as chemosensors in a similar way as taste buds and photoreceptors. However, because carotid and aortic bodies detect variation within the body's internal organs, they are considered interoceptors. Taste buds, olfactory bulbs, photoreceptors, and other receptors associated with the five traditional sensory modalities, by contrast, are exteroceptors in that they respond to stimuli outside the body. The body also contains proprioceptors, which respond to the amount of stretch within the organ, usually muscle, that they occupy.
As for their particular function, peripheral chemoreceptors help maintain homeostasis in the cardiorespiratory system by monitoring concentrations of blood borne chemicals. These polymodal sensors respond to variations in a number of blood properties, including low oxygen (hypoxia), high carbon dioxide (hypercapnia), and low glucose (hypoglycemia). Hypoxia and hypercapnia are the most heavily studied and understood conditions detected by the peripheral chemoreceptors. Glucose is discussed in a later section. Afferent nerves carry signals back from the carotid and aortic bodies to the brainstem, which responds accordingly (e.g. increasing ventilation).
Both carotid bodies and aortic bodies increase sensory discharge during hypoxia. Carotid bodies are considered the primary peripheral chemoreceptor and have been shown to contribute more to a hypoxic response. However, in the chronic absence of the carotid body, the aortic body is able to perform a similar respiratory regulatory role, suggesting that it possesses efficacious mechanisms of signal transduction as well. The differing locations of the two bodies ideally position them to take advantage of different information; the carotid bodies, located on one of the main arteries of the neck, monitor partial pressure within arterial vessels while aortic body, located on the aortic arch, monitors oxygen concentration closer to the heart. Each of these bodies is composed of a similar collection of cells, and it is the post-transduction signal processing that differentiates their responses. However, little is known about the specifics of either of these signaling mechanisms.
Carotid and aortic bodies are clusters of cells located on the common carotid artery and the aortic arch, respectively. Each of these peripheral chemoreceptors is composed of type I glomus cells and glia-like type II cells. The type-I cells transduce the signals from the bloodstream and are innervated by afferent nerve fibers leading back to (in the carotid body) the carotid sinus nerve and then on to the glossopharyngeal nerve and medulla of the brainstem. The aortic body, by contrast, is connected to the medulla via the vagus nerve.
They also receive input from efferent nerve fibers leading back to the same set of nerves. The entire cluster of cells is infiltrated with capillaries to provide access to the bloodstream; the high capillary density makes this one of the areas of the body with the greatest blood flow. Type I cells are densely packed with vesicles containing various neurotransmitters, including dopamine, ATP, serotonin, catecholamine, released during transduction. Type I cells are often connected via gap junctions, which might allow for quick communication between cells when transducing signals.
Type II cells occur in a ratio of about 1 to 4 with type I cells. Their long bodies usually occur in close association with type I cells, though they do not entirely encase type I cells. They lack the vesicles of type I cells used in neurotransmitter communication, but studies indicate they function as chemoreceptor stem cells and can respond to prolonged exposure to hypoxia by proliferating into type I cells themselves. They may also bolster rapid communication among type I cells by amplifying release of one of the primary neurotransmitters in chemoreceptive signaling, ATP.
Sensitivity and physiology of the peripheral chemoreceptors changes throughout the lifespan.
Respiration in neonates is irregular, prone to periodic breathing and apnea. In utero and at birth, the carotid body's response to hypoxia is not fully developed; it takes a few days to a few weeks to increase its sensitivity to that of an adult carotid body. During this period of development, it is proposed that neonates heavily rely on other oxygen-sensing chemoreceptors, such as the aortic body or central chemoreceptors. However, non-carotid body chemoreceptors are sometimes not enough to ensure appropriate ventilatory response; SIDS deaths occur most frequently during the days or weeks in which the carotid body is still developing, and it is suggested that lack of appropriate carotid body activity is implicated in this condition. SIDS victims often are reported to have displayed some of the characteristic troubles in carotid body development, including periodic breathing, much sleep apnea, impaired arousal during sleep, and low sensitivity to hypoxia. The carotid bodies of SIDS victims also often display physiological abnormalities, such as hypo- and hypertrophy. Many of the findings on to carotid body's relation to SIDS report that carotid body development is impaired by environmental factors that were already known to increase the risk of SIDS, such as premature birth and exposure to smoke, substances of abuse, hyperoxia, and hypoxia, so it may seem initially as if carotid body studies are only extending what we know about SIDS into another domain. However, understanding the mechanisms that impair carotid body development could help elucidate how certain aspects of neonatal, particularly premature, care might be improved. For example, oxygen therapy may be an example of a technique that exposes premature infants to such high oxygen levels that it prevents them from acquiring appropriate sensitivity to normal oxygen levels.
Peripheral chemoreceptor
Peripheral chemoreceptors (of the carotid and aortic bodies) are so named because they are sensory extensions of the peripheral nervous system into blood vessels where they detect changes in chemical concentrations. As transducers of patterns of variability in the surrounding environment, carotid and aortic bodies count as chemosensors in a similar way as taste buds and photoreceptors. However, because carotid and aortic bodies detect variation within the body's internal organs, they are considered interoceptors. Taste buds, olfactory bulbs, photoreceptors, and other receptors associated with the five traditional sensory modalities, by contrast, are exteroceptors in that they respond to stimuli outside the body. The body also contains proprioceptors, which respond to the amount of stretch within the organ, usually muscle, that they occupy.
As for their particular function, peripheral chemoreceptors help maintain homeostasis in the cardiorespiratory system by monitoring concentrations of blood borne chemicals. These polymodal sensors respond to variations in a number of blood properties, including low oxygen (hypoxia), high carbon dioxide (hypercapnia), and low glucose (hypoglycemia). Hypoxia and hypercapnia are the most heavily studied and understood conditions detected by the peripheral chemoreceptors. Glucose is discussed in a later section. Afferent nerves carry signals back from the carotid and aortic bodies to the brainstem, which responds accordingly (e.g. increasing ventilation).
Both carotid bodies and aortic bodies increase sensory discharge during hypoxia. Carotid bodies are considered the primary peripheral chemoreceptor and have been shown to contribute more to a hypoxic response. However, in the chronic absence of the carotid body, the aortic body is able to perform a similar respiratory regulatory role, suggesting that it possesses efficacious mechanisms of signal transduction as well. The differing locations of the two bodies ideally position them to take advantage of different information; the carotid bodies, located on one of the main arteries of the neck, monitor partial pressure within arterial vessels while aortic body, located on the aortic arch, monitors oxygen concentration closer to the heart. Each of these bodies is composed of a similar collection of cells, and it is the post-transduction signal processing that differentiates their responses. However, little is known about the specifics of either of these signaling mechanisms.
Carotid and aortic bodies are clusters of cells located on the common carotid artery and the aortic arch, respectively. Each of these peripheral chemoreceptors is composed of type I glomus cells and glia-like type II cells. The type-I cells transduce the signals from the bloodstream and are innervated by afferent nerve fibers leading back to (in the carotid body) the carotid sinus nerve and then on to the glossopharyngeal nerve and medulla of the brainstem. The aortic body, by contrast, is connected to the medulla via the vagus nerve.
They also receive input from efferent nerve fibers leading back to the same set of nerves. The entire cluster of cells is infiltrated with capillaries to provide access to the bloodstream; the high capillary density makes this one of the areas of the body with the greatest blood flow. Type I cells are densely packed with vesicles containing various neurotransmitters, including dopamine, ATP, serotonin, catecholamine, released during transduction. Type I cells are often connected via gap junctions, which might allow for quick communication between cells when transducing signals.
Type II cells occur in a ratio of about 1 to 4 with type I cells. Their long bodies usually occur in close association with type I cells, though they do not entirely encase type I cells. They lack the vesicles of type I cells used in neurotransmitter communication, but studies indicate they function as chemoreceptor stem cells and can respond to prolonged exposure to hypoxia by proliferating into type I cells themselves. They may also bolster rapid communication among type I cells by amplifying release of one of the primary neurotransmitters in chemoreceptive signaling, ATP.
Sensitivity and physiology of the peripheral chemoreceptors changes throughout the lifespan.
Respiration in neonates is irregular, prone to periodic breathing and apnea. In utero and at birth, the carotid body's response to hypoxia is not fully developed; it takes a few days to a few weeks to increase its sensitivity to that of an adult carotid body. During this period of development, it is proposed that neonates heavily rely on other oxygen-sensing chemoreceptors, such as the aortic body or central chemoreceptors. However, non-carotid body chemoreceptors are sometimes not enough to ensure appropriate ventilatory response; SIDS deaths occur most frequently during the days or weeks in which the carotid body is still developing, and it is suggested that lack of appropriate carotid body activity is implicated in this condition. SIDS victims often are reported to have displayed some of the characteristic troubles in carotid body development, including periodic breathing, much sleep apnea, impaired arousal during sleep, and low sensitivity to hypoxia. The carotid bodies of SIDS victims also often display physiological abnormalities, such as hypo- and hypertrophy. Many of the findings on to carotid body's relation to SIDS report that carotid body development is impaired by environmental factors that were already known to increase the risk of SIDS, such as premature birth and exposure to smoke, substances of abuse, hyperoxia, and hypoxia, so it may seem initially as if carotid body studies are only extending what we know about SIDS into another domain. However, understanding the mechanisms that impair carotid body development could help elucidate how certain aspects of neonatal, particularly premature, care might be improved. For example, oxygen therapy may be an example of a technique that exposes premature infants to such high oxygen levels that it prevents them from acquiring appropriate sensitivity to normal oxygen levels.